So this afternoon, we're gonna look at anaesthesia monitoring for our patients. There's lots of methods available now for monitoring under anaesthesia, and I think as clinical staff, we need to be aware not only of the benefits of those monitors, but also the limitations and the information that they can't give us. It's really vital that we don't monitor the monitors, and we use them instead as additional tools to support our hands-on monitoring.
That being said, the level of monitoring that we have available now does enhance and promote safety for our patients. So if you have monitors, then do use them, but just bear in mind their limitations and also don't forget the hands-on monitoring, which is a vital part of monitoring our patients under anaesthesia. So we're really looking at cardiovascular monitoring.
We do look at respiratory system as well a bit later in this webinar. And we're looking at indicators of circulation. So we want to look at heart rate and pulse rate and quality.
We want to know if our patient is developing pulse deficits, for example, under anaesthesia. We would monitor heart rhythm using an ECG. We would look at mucous membrane colour and capillary refill time.
They will give us good indicators of if the patient is becoming hypovolemic, has a hyperdynamic response is in SERS or sepsis, where their capillary refill time is much more rapid. We will also look at blood pressure. Obviously, we encounter various problems with blood pressure maintenance under anaesthesia, and it's important that we know how to address those.
Our indicators of oxygenation are gonna be mucous membrane colour, but equally, we don't see cyanosis develop in our patients until the PAO2 is very, very low. So the patient could be hypoxemic without you having a change in mucous membrane colour. We can look at pulse oximetry and also blood gas analysis for these patients to try and make the anaesthetic process and the monitoring that we do as safe as possible for them.
So when we think about the pulse oximeter, it's a pretty universal piece of kit. We all have one of these in practise, I would imagine. And if you're anything like me, it's one of those things that you have a love-hate relationship with.
Most of the time I love it, sometimes I hate it, because it does have these problems associated with it. And they're normally patient problems. So the way it works, we have an infrared light that emits from one side of the probe with a sensor on the other side, and that detects light going through pulsatile tissues.
If we shine a light through tissue, some areas are going to constantly absorb light, but they might have to pass through skin, muscle, etc. The amount of venous blood is usually fairly consistent in the short term, but long term, that volume can change. So if you have, for example, a patient that is having a long anaesthetic, so over half an hour, for example, you might need to reposition the probe because we get some compression of that vascular tissue bed, which leads to pulsar blood flow changing.
The volume of arterial blood changes over the cardiac cycle, so we will get different absorption of light, and that's how our pulse rate is measured. So generally, if you have an accurate heart rate showing on your pulse ox, then you can consider the SPO2 reading as being accurate. What does it rely on?
Well, it relies on, as we've said, pulse tar blood flow. It also relies on patients having adequate haemoglobin transported around the body to carry oxygen. So it's actually measuring the amount of haemoglobin saturated with oxygen.
The potential complications movement. Does cause us issues flickering lights overhead, pigment and hair. So we often use this in conscious patients, but if there are hair or pigment in the way on the lips or the ears, that can cause us a problem.
Coression of tissues, so compression of that pulsatile blood flow, or alteration of blood flow. We can have misaligned probes, and we can also encounter other forms of haemoglobin. So ultimately, what we're looking at with this is if we have a heart rate that is accurate on the pulse ox.
And we're sure there are no other forms of haemoglobin present. Then we can look at pigment or hair is causing a problem. Is the patient moving excessively?
Have we got a flickering light overhead that's interfering with the signal that we're getting from the machine? So if the SPO2 is falling, we can absolutely trust the reading if it's placed on well-perfused, non-pigmented, non-compressed tissues. What we would generally do in that situation under anaesthesia would be obviously to inform the veterinary surgeon.
Check our oxygen supply or administer 02. Check the placement of the endotracheal tube, so checking it's not obstructed or kinked. Check our respiratory rate, depth and pattern is our patient hypoventilating, causing an alteration in gaseous exchange in the lungs.
If we're using nitrous oxide, then we would discontinue that and we can also use the Capnograph to help us identify where the problem is. Sometimes the SPO2 monitor falling, numbers falling, is something as simple as repositioning the probe. So we've got a bit of compression of tissues and we need to reposition the probe.
Situations where the pulse ox doesn't work terribly well are patients that are anaemic, so they have that low haemoglobin level. They've got a reduction of red blood cells. So we're not gonna get as accurate a reading on those.
If we've got patients arrhythmias, because it relies on pulsar blood flow to be accurate, we may not get accurate measures on those, and patients that are vasoconstricted, hypovolemic or hypothermic, we might encounter issues actually picking up a pulse in the first place. Our next monitor that we have during anaesthesia is blood pressure, and we monitor this obviously at a lot of other times as well. It's maintained in two ways.
So we can look at the normal physiological processes to maintain blood pressure. We have barroceptors which are located throughout blood vessels and adjust our heart rate and contractility as required. So they take care of the day to day adjustments in blood pressure.
That we need. We can also see vasoconstriction and dilation to maintain blood pressure in the normal range. We have, the kidneys, which will offer general homeostasis.
So if we have an increase of blood volume, they'll excrete extra blood volume or extra water and sodium. If we have decreased blood blood volume, we'll get retention of those things. Blood pressure is one of those things that we should consider important in all of our patients, but especially under anaesthesia.
Some of the agents that we use can have profound effects on blood pressure. A prime example of that is meatomidine, where we get that biphasic. Initial increase in blood pressure and then a decrease just back down to below normal alongside a bradycardia.
Some of our inhaling agents, so things like isofluorine and sevoflurane, can profoundly affect blood pressure. And one of the things that we look at when we have a patient that's hypotensive under anaesthetic is can we reduce the inhaling agent at all. There are several ways to measure blood pressure.
We can use a direct or invasive approach, so that involves placing an arterial line with a transducer, and the measures are then displayed on a screen. The advantage of direct monitoring is it gives us beat by beat information about what the patient's blood pressure is doing. The disadvantage is it does take some skill to set up.
Of course, you need the correct equipment, . And there can be more complications associated with the arterial line, similar to placement of a venous catheter, but we can see obviously significant haemorrhage from arterial lines. More commonly, we use the indirect or noninvasive methods.
So we use a Doppler or an oscillometric monitor. And what we're using there is a cuff. We get occlusion of flow, and then we measure the blood pressure when that flow returns to the vessel.
And that's done in a couple of different ways. . So when we think about the oscillometric monitor, We need to use a single or a double tubed cuff.
The size must be appropriate for the patient. If the cuff is too large, then we'll get an overreading of blood pressure. If it's too small because the cuff will be under more pressure, we'll get under reading of that.
The pump inflates the cuff and then air is permitted to escape. We get oscillations detected with the oscillometric. So they detect the systolic oscillations and they disappear with the diastolic.
The most accurate reading on an oscillometric monitor is going to be your mean arterial pressure. So, We can have multiple readings from these patients. We can monitor trends from them during anaesthesia.
We can even print them out from multiparameter machines if we need to for their anaesthetic records. Ideally, you would be looking at your mean arterial pressure if you're using an osciometric monitor. When we think about the Doppler, we use this quite universally, especially in smaller patients, in cats, it seems to be a lot more accurate.
Both of them will struggle with patients that have arrhythmias. We might have problems obtaining a reading in some patients if they're very, very vasoconstricted, if they're hypovolemic, or in another form of shock. When we think about the Doppler, we're all familiar with this, but it's just a cuff that we use a sphonometer to inflate.
We then decrease that to using the sphagonometer until we hear an audible sound. So the audible sound we get with the Doppler is the systolic blood pressure. In cats, it potentially could be closer to their mean arterial pressure.
Was a study done not long ago that compared Doppler with direct arterial blood pressure monitoring. And they identified that in anaesthetized or sedated cats, that the blood pressures with direct monitoring were much closer in correlation to the Doppler. Reading we will get as a systolic.
So something to bear in mind if you're anaesthetizing cats, is that you might be Hearing the mean arterial pressure on your Doppler rather than the systolic. C positions are important. Ideally, we want them to be in line with the heart.
So we look at a position above the carpus, below the heart, around the tail. Others are possible, and I think the important thing is that we record it. So if we've taken a blood pressure reading, we record where we're taking that reading from so that we have some consistency going forwards and we can monitor trends in blood pressure for that patient.
The limitations of the oscillometric method, we're looking at very small animals for some monitors. The, the newer monitors are much better now. But previously, we wouldn't use them on anything below 5 kg.
Patients that have irregular or slow pulse rates can cause us an issue. Patients with lots of hair and feathers, might need those clipped off so that we get good contact. Your cuffs might slip and movement can be a problem.
So, cuff size, we've already discussed that, but we normally measure 40% of circumference of the limb for the width of the cuff. If we get a too large cuff, then we get an under reading and too small, we get an overreading. So we get false information that might be relevant to our patients.
The Doppler, as we've said, is a single tube cuff. We use a manual inflation with the gauge figonometer, and the Doppler probe detects return of blood flow, mainly systolic, but there is that information about cats and potentially being their mean arterial pressure. There is also some discussion as to whether some people can hear diastolic.
We don't think that's the case, just that The systolic is the most accurate measure. Some people might hear the diastolic, but there's not been enough research done as to whether that is going to be accurate or not. Other uses for the Doppler probe, we can use it during resuscitation.
There's no point in attaching a blood pressure monitor to your patient if they are in cardiopulmonary arrest because they don't have a cardiac output. So you're not gonna hear anything except movement. Oscillations.
One thing that you can do with the Doppler probe though is use some coupling gel and stick it onto the cornea with some tape, and that will give you an audible sound of retinal blood flow. So if your compressions are adequate, you should hear a pulse for every compression that you're doing. The other potential use for a Doppler is detecting blood flow to an appendage.
So if we have, for example, a Patient with a thromboembolism, aortic thromboembolism, and we want to check whether we've got blood flow. We can test that using the Doppler. We can use a normal Doppler to assess whether there is blood flow.
So just a quick review of the advantages and disadvantages with the non-invasive measurements, everybody's got access to that. It's easy to apply. It can be used in small animals and it's going to be universally available more or less.
The disadvantages is that they are intermittent, with the Doppler, obviously you have to manually inflate and deflate the cuff with the osciometric. It's not a continuous reading. We normally set the timer to every 5 minutes.
It is potentially less accurate. And there is a risk of pressure damage or interference with blood flow, so we should always give a period of time of about 30 seconds to 1 minute to allow blood flow to return to the limb before we actually take another reading. With invasive measurements, we have several advantages.
We've got the accuracy. So it is by far the gold standard for accuracy, and we get beat by beat changes which we don't get with the non-invasive measurements. Disadvantages obviously are risks of arterial catheterization.
It can be challenging in some patients. It does need more expensive equipment and it needs careful set up if you're going to ensure that your readings are accurate. When we talk about blood pressure, what are we talking about in terms of hypotension?
Well, we look at hypertension as a systolic pressure of less than 90. A mean arterial pressure of less than 60 or 65. And in those situations, our tissue perfusion, such as delivery of oxygen to the tissues, is severely reduced.
We've got issues with perfusion of the kidneys and the brain as well. So we end up with a patient that has poor perfusion, delivery of oxygen, leading to hypoxia and acidosis. Normally they're gonna be associated with a reduction in cardiac output or fluid loss during surgery, leading to reduction of cardiac output, so hypovolemia, or we might have reduced systemic vascular resistance, with our systemic inflammatory response syndrome patients or our patients with sepsis.
So in that case, we get vasodilation and the patient is unable to maintain their own arterial blood pressure. When we think about how we manage those situations, well, we would look at what is the cause first of all, if we've got a reduction in cardiac output because of hypovolemia, then fluid bonuses are gonna be our most appropriate course of action, as well as reevaluating pain. And other parameters.
If we think that we have systolic dysfunction, so if the heart is not contracting properly and injecting blood properly, we might look at inotropes to improve systolic function. If we've got vasodilation, so if we have a systemic inflammatory response patients, we would look at vasopressors. So something like norepinephrine, sometimes dibutymine, dopamine might be used if you don't have access to norepi.
So there are several things that can cause a problem, and there are several ways in which we can manage them. But they all come down to us identifying that the patient has a problem in the first place. ECG basics, so the ECG is one thing that I find people really struggle with quite a lot.
And I would say it's not as difficult as we think it is. It allows us to carry out clinical monitoring of a patient that perhaps has arrhythmias, has tachycardias, or is under anaesthetic and at risk from those things. When we think about the ECG, it's important to remember it's purely measuring the electrical activity in the heart.
It doesn't tell us if the patient is having issues with contractility. It doesn't tell us if the patient is in heart failure. It will literally tell us just the rate and the rhythm, and if there is abnormality in conduction of electrical signals that are leading to arrhythmias.
We can see problems with it. So when everything's working as it should be, and that's where we get our kind of basic heart rates for dogs and cats from, The sinoatrial node is the pacemaker for the heart. So we get a heart rate maybe of around 100 to 140 in small dogs, maybe 60 to 100 in large dogs.
It will depend also on how physically fit the patient is. We always kind of say a range of 60 to 160 for a large dog and 80 to 180 for a small dog, but I think once we kind of get to the point of 160, we should be concerned that something is abnormal. It could be pain, it could be hypovolemia, it can be stress, it can be anxiety, but it's really not unusual for a calm, healthy patient to have heart rates that are sustained at 160.
With cats, we normally think of the 160 to 200 range, If we have a patient in the hospital that has a heart rate of 120 or 140, it always bothers me a little bit if they're cats because I do think that that is probably bradycardic when they, when we think about cats and how anxious they get when they're in the hospital environment. So when we think about the cardiac cycle, we have transmission of electrical impulses in two ways. We've got the specialist conduction system so that governs how the heart contracts and also direct cell to cell transmission.
So if we get interference with either of these systems, we'll start to see problems developing on our ECG. So the sinoatrial node, as we've said before, it's the primary pacemaker for the heart. The AV node could be classed as your secondary pacemaker.
If something happens and the sinoatrial node fails, for example, Then the AV node takes over. So the problem with that is that it doesn't fire at the same rate as the SA node. So it has its own intrinsic rate, which is much lower.
It may be different for individuals, but the ballpark figures are in dogs. It can be as low as 40 to 80. In cats, it might be the 130 to 150 range.
So if your conduction system is really broken and your sinoatrial node and AV node are not working, then the ventricles will start to try to fire randomly. The ventricles just try to maintain cardiac output. The further down in the conduction train your primary pacemaker is, the slower that intrinsic rate will be.
And certainly ventricular arrhythmias are very obvious on our ECG because we miss out two parts of the conduction system that we normally look at. So our normal ECG formation is very, very simple. So I think this is where we get into issues where we perhaps make it a little bit more complicated.
So we have the P wave, which is the atrial depolarization. If you're missing a P wave, there is something wrong with the atria. So with the sinoatrial node, the AV node, potentially an electrolyte imbalance caused by anaesthesia or something along.
Those lines. The QRS is activation of the ventricles. So if you see changes in height or pattern in those, then we've got an issue with the ventricles.
And then the T wave is repolarization or recovery wave for the heart. So it's a resting phase. So we can see that 3 different Complexes will tell us about the activity of the three different areas of the heart.
Each cardiac cycle must have a P wave followed by a QRS complex, followed by a T wave in a healthy patient. So when we think about if the ECG is normal, we can follow a logical sequence. So we can look at the rate.
Is it fast, slow or normal? Have we got normal regularity, so are the RR intervals equal? Do we have a sinus arrhythmia?
We can look at the order. So we do, do we have a P for every QRS complex and T wave? And are all our QRS complexes the same height.
And this will give us more information about what's going on. But ultimately, when we assess an ECG, this is what we're looking for. As we've said, irregularity or lack of a P wave will indicate an atrial problem.
It could be an AV block, it could be an electrolyte abnormality. We need to identify what's causing the issue and what we can do about it. Irregularity or lack of ac.
URS complex is gonna indicate a ventricular problem. So we need to look at those components individually and also the patient we have in front of us to identify what the issue is, if we need to do something about it, and if so, what are we gonna do about it? Arrrhythmias under anaesthesia are really, really common.
Causes are anaesthetic drugs, pain, hypoxia, direct trauma to the myocardium, so direct trauma to the heart can lead to ischemic injuries. Electrolyte imbalances, the most common ones you're going to encounter problems with are your potassium and also calcium, causing abnormalities in heart rate and rhythm. Head trauma patients might have arrhythmias.
Especially under anaesthesia, patients with splenic masses and GDVs very, very commonly have premature ventricular contractions. In fact, any patient having acute abdomen surgery can have those, and we might see arrhythmias developing because of hypothermia as well. So there are lots of things to consider when we think about ECG.
And ultimately what we're looking at is identifying whether that arrhythmia is affecting the patient's cardiac output. Is our blood pressure falling? Is our Nidal CO2 falling, which indicates a drop in cardiac output?
Can we palpate a pulse? If so, do we have a good pulse quality or is it feeling a little bit weaker than it was initially? Can we place a Doppler?
To listen to the pulse quality, do we have pulse deficits? So when we consider if the end tidal CO2 is falling, an indirect use of catography is an indicator of cardiac output. If ventilation hasn't changed, so if your patient is still breathing and it's firing gas normally, if cardiac output falls and tidal CO2 will fall with it.
The other thing we can look at with arrhythmias is how often are they occurring. So if we're seeing perhaps 1 VPC a minute, we probably wouldn't be too worried about it. Whereas if we're seeing 8 or 10, we're gonna have to act on that.
Consider the things that might have an impact on patient's heart rhythm. So things like anaesthetic drugs, hypoxia is your patient on 100% oxygen. Pain, inadequate depth of anaesthesia might be a problem, presenting complaint or the reason for the anaesthetic in the first place, and electrolyte disturbances as well.
So there are various things that cause cause arrhythmias under anaesthetic. Some of them we do something about, some of them we don't. The important thing is to be able to recognise them.
So the common cardiac arrhythmias are a sinus bradycardia. We might see an inappropriate bradycardia in some patients because of the anaesthetic drugs that we've used, we potentially can see AV block developing as well, particularly common with meatomidine in my own experience, . And it's important that we monitor for those.
When I think about bradycardia, if I've got good pulse quality, good cardiac output, good blood pressure, and our endide or CO2 is normal, then I don't worry about it too much. But if any of those other parameters have changed, then we would start thinking about what we need to do. Tachycardia can come in various forms, so we can see just a normal tachycardia associated with pain, hypovolemia, stress, anxiety, .
Inadequate plane of anaesthesia. We might see ventricular premature complexes, so it's like an escape beat from the ventricles associated, particularly with acute abdomens, but we can see them for a number of other conditions as well. Ventricular tachycardia occurs when we have Just QRS complexes on our ECG.
So we don't have a P-wave normally. We don't have a T wave. There's no rest period for the heart.
There's no depolarization. We just have the ventricles firing at random, to try and maintain cardiac output. They can only do that for a very, very short period of time, and we have to address ventricular tachycardia rapidly.
Because it will cause us major problems with our patients. It's normally controlled by assessing the issues that might be causing a problem, so hypovolemia, pain, inadequate depth of anaesthesia, monitoring blood pressure, but also giving lidocaine as an anti-arrhythmic, and we do need to address it very quickly if it occurs. When we think about assessment of ventilation, there are various things we can look at.
Blood gas analysis is going to be our kind of gold standard for measuring ventilation, and it's certainly needed to measure hypoxemia, but it does come with problems in that it's invasive, it's technical, and it's more expensive. So as we've discussed before, it would involve placing an arterial line, if we're going to do repeated blood gas measurements. And it can be quite challenging to maintain those.
One of the things that we can think about is in a healthy patient with normal lung normal lung function, our Nidal CO2 correlates very, very closely. To our PACO2, that should read. So it's normally about 2 to 5 millimetres of mercury lower.
So it's a fairly reliable indicator in patients with adequate lung function of what the CO2 level is doing. A change in endide or CO2 suggests an alteration in one or more of the following parameters. It can be an alteration in systemic metabolism.
It can be an alteration in cardiac output, and it can be an alteration in pulmonary perfusion. So it doesn't just give us information about the patient's ability to ventilate, it also gives us some information about their cardiovascular system stability and their metabolic stability. So capnography is far superior to pulse oximetry and identifying apnea, identifying airway issues.
Any changes are seen on the capnograph instantly because we get a breath by breath waveform, . Indications for canography in veterinary patients are massive. We can use it for any number of patients, but ultimately they they're normally used for monitoring of ventilation in spontaneously breathing anaesthetized patients, monitoring for patients undergoing mechanical ventilation.
Monitoring of patients undergoing CPR, monitoring of patients. That are intubated but comatose. We can also use it to confirm endotracheal tube placement and also nasal esophageal feeding tube placement because we don't have any CO2 in the oesophagus.
So if our catnograph, if our feeding tube is in the right place, then the Capnograph reading will be very low to 0. There are two types of trapnograph. We have the mainstream and the side stream capnographs.
So a sensor from the monitor is attached to the endotracheal tube in the mainstream one, and the end tidal CO2 measurement is taken from the sensor at the exit of the endotracheal tube. We'll get a numerical value and a wave form displayed on the monitor. Issues with the monitor, they require a warm up period and they will often require frequent calibration during use for accuracy and that might be unsuitable in emergency patients.
When they use long term. The sensor is heated to prevent the accumulation of moisture and condensation from exhaled gases, so when they use long term, those inhaled gases may be heated by the sensors sufficiently to pose a risk of burns to respiratory tissues. When we think about the addition of sensors attached to breathing circuits in small patients, for example, that might add to space and the the dead space and the weight attached to the tubing.
So we might encounter issues from that. With the side stream, a sampling tube from the monitor is attached to the endotracheal tube and a sample of expired gas is collected from the exit of the endotracheal tube. To the capometer where the end tidal CO2 level is measured.
Again, we get a numeric value and also a wave form, which are displayed on a monitor. Some of the side stream monitors will require increased oxygen flow rates, because the capometer draws off a portion of gas to take its measurement. The small bore size.
Of the sampling tube might become a problem with respiratory secretions, causing inaccurate readings. Moisture caused by condensation can also interfere with those readings. So they are things to be aware of when you're using the different types of tanographs.
When we think about how to interpret the catnogram, we can look at a regular waveform. So we'll come on to the next slide in a moment, but we get a waveform with these catometers. Does the waveform return to baseline?
So does it return to zero, where we've got an animal breathing 100% oxygen, or is there evidence of re-breathing? Is the angle of the upstroke normal, or have we got slow exploration? So a slanted upstroke, it should be a steep upstroke.
Is the alveolar plateau normal or is there evidence of uneven emptying? Are our end tidal CO2 values within an acceptable range? And are they consistent with the patient's respiratory parameters?
And then we also look at the angle of the downslope as well to see if there is evidence of problems with inspiration or rebreathing. So have we got a slanted down stroke for those patients? So the numerical readings we're all used to, we get those Showing on the screen commonly in dogs on normal levels of 35 to 45 in cats 28 to 35.
So how do we know when we've got a problem? Well, we get an increased tide or CO2. With hypoventilation.
So That occurs either due to increased CO2 production because of increased metabolism, we might have issues with increased depth of anaesthesia. We might have problems with patients with hypothermia or seizure activity causing hypoventilation. If we have a value over 50 millimetres of mercury, then that would indicate inadequate ventilation and ventilatory assistance via manual or mechanical means is required.
If the Nidal CO2 is above 60, which I wouldn't recommend leaving until that point, you've got a patient with an acidosis. So the knock-on effect of that is it's gonna affect our cardiac output. It's gonna affect the patient's ability to maintain body temperature.
It will affect blood pressure and we need to address it before it gets to that stage. When we think about decreases in tidal CO2, it's often gonna be indicating hyperventilation or decreased CO2 production because of decreased metabolism. So hypothermia is one of the indications we might have for that.
We might have decreased cardiac output as well. A sudden drop in CO2. So if you're monitoring your catnograph and your CO2 suddenly drops to zero, then we need to think about if the patient has gone into cardiac arrest or if we have a pulmonary embolism, which can obviously occur in our patients.
Zeroentide or CO2s might also indicate esophageal intubation, endotracheal tube disconnection, cardiac or respiratory arrest, apnea, misplacement of the endotracheal tube, extubation, disconnection of the breathing circuit, or an airway obstruction. So there are lots of things we can troubleshoot if we encounter problems with our Nidal CO2. But the most important thing is, firstly, assess your patient.
Look at their breathing. Are they breathing normally? Are they breathing much more slowly than normal?
Have we got good chest movement indicating that ventilation should be appropriate, or is it excessive or non-existent indicating that we have a major problem? So our normal catnograph trace, it's important we understand this kind of normal trace before we start to try and interpret abnormal ones. So when we look at the trace, we have a 0 here, which is where the patient is breathing in 100% oxygen.
This is our upstroke for expiration, so they start to breathe out CO2. The alveolar plateau, so the point at which the CO2 level will be the highest, slants upwards slightly at the end of expiration. And then as the patient starts to breathe in again, this line should return to 0, indicating that they're breathing in 100% oxygen.
So when we think about hypoventilation, one of the waveforms that we can see, obviously we'll get the numbers reported, but the waveforms are very useful too. We get a normal shape on the Kapnograph, but a higher end tidal CO2 might be 50 to 60. Most common reason is going to be too deep under anaesthesia, decrease your inhalant setting if you possibly can, or potentially IPPV depending on how high that number is.
That number is. We might need to think about IPPV if we get above 50, and certainly if it's anywhere near 60, we would look at ventilating that patient to bring it back down to a normal range. With hyperventilation, again, we have a normal wave form, but we have a drop in CO2 levels, so the patient.
It probably has a decreased CO2 production that can be because of decreased metabolism. So hypothermia is really common in our anaesthetized patients or decreased cardiac output. So it's important we evaluate those things and act on them if they are present.
Rebreathing of CO2 can occur. It's normally an equipment problem. So we see with the circles we get exhausted social lines.
With non-rebreathing circuits, it can be inadequate fresh gas flow rates. We can get increased dead space, so check our endotracheal dead space, especially in our smaller patients. We can also see this with sticky one-way valves on a circle circuit.
Cardiac oscillations are a normal form as the patient breathes in. We get oscillations from the beating of the heart. So this kind of oscillation downwards on the inspiratory slant down is completely normal and nothing to worry about.
Just finally to finish off, obviously, we Have all of these monitors. One of the really important things that we can monitor in these patients is body temperature. We do have problems with maintaining body temperature under anaesthesia, and it's really important we understand why that's important.
So if the temperature becomes too low, we will get patients that are not able to metabolise drugs properly. So we then get delayed recovery from anaesthesia. We get poor immune system function.
We can see coagulopathies developing because as they get cold, their blood becomes thicker and more viscous. We get hypercoagulable states. So with body temperature, we try and maintain it as much as possible before anaesthesia, during and also aggressively afterwards if we need to.
And we should really be monitoring these patients until their body temperature is back to normal, if it's abnormal when they are in recovery from an anaesthetic. So, in summary, anaesthesia monitoring has to be performed regularly on every anaesthetized and sedated patient. We know we need to fill in our anaesthetic monitoring charts and ideally we'd be filling in, surgical checklists as well that can give us an overview of anaesthetic monitoring for that individual patient.
Don't forget your basic hands-on monitoring though. There are lots of things that you can pick up much much more quickly than machines can. But also things that you can identify with hands-on monitoring that the machines can't tell you.
We can gain confidence and knowledge in utilising anaesthesia monitoring techniques. There are lots and lots of detailed websites and information online. Looking at ECGs and capnography, for example.
So if you wanted more information, then I do suggest you go and look for those. You are welcome to contact me with any questions if you need to on Katherine. Howie at vetsow.com.
Thank you for listening. I hope you found this useful, and thank you to the webinar vets.
